Researchers at the Department of Military and Emergency Medicine in Bethesda, MD investigated the effects of alcohol and caffeine on HSP72 induction and oxidative stress in mice. According to other studies, alcohol intake is linked to organ dysfunctions seen in the liver, the heart and skeletal muscle.  Alcohol-induced oxidative stress has been postulated as a mechanism for these effects, due to an accumulation of toxic metabolites found in the tissues previously mentioned.  When confronted with this type of insult, cells will rapidly synthesize the inducible form of HSP70 (HSP72).  However, there is evidence that it is not the oxidative stress that induces this rapid synthesis, but the structural damage done to the cell by other means.  So these researchers decided to measure inflammatory and oxidative activities, HSP72 levels and structural changes in these tissues.

Three groups of mice were examined over ten consecutive days.  The three groups were given either: acute large doses of alcohol, similar doses of caffeine or a combination of the two.  The administration of caffeine alone did not seem to affect any of the tissues analyzed.  It seems that administration of alcohol, as well as alcohol and caffeine, led to lesions in the heart, liver and gastrocnemius muscle.  Not surprisingly, it seems that the liver is more sensitive to induction of HSP72 by alcohol than other tissues.

Interestingly, alcohol alone led to decreased glutathioine levels in all three tissues and reduced plasma superoxide dismutase (SOD) capacity; whereas administration of alcohol with caffeine did not affect these levels in the heart, nor did they affect the SOD capacity. This may suggest that the caffeine can mitigate some of the damaging effects of alcohol; though this seems to be dependent on the dose of caffeine, as purported by other studies.

The authors take these findings to suggest that a redox mechanism is involved with the structural impairments caused by alcohol.  Further, oxidative tissue injury may not be linked to HSP72 induction.  They conclude that HSP72 induction is mediated at both the transcriptional and translational levels.

The original research paper was published in Cell Stress and Chaperones, March 2013:

Tissue-Specific Upregulation of HSP72 in Mice Following Short-Term Administration of Alcohol.